Evidence map›Paper›PMID 26522723›Full record

ArticleOncogene2016

The homeoprotein DLX3 and tumor suppressor p53 co-regulate cell cycle progression and squamous tumor growth.

E Palazzo, M Kellett, C Cataisson, A Gormley, P W Bible, V Pietroni, N Radoja, J Hwang, M Blumenberg, S H Yuspa and 1 more

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 29 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

E PalazzoLaboratory of Skin Biology, NIAMS, NIH, Bethesda, MD, USA.
M KellettLaboratory of Skin Biology, NIAMS, NIH, Bethesda, MD, USA.
C CataissonLaboratory of Cancer Biology and Genetics, NCI, NIH, Bethesda, MD, USA.
A GormleyLaboratory of Skin Biology, NIAMS, NIH, Bethesda, MD, USA.
P W BibleLaboratory of Skin Biology, NIAMS, NIH, Bethesda, MD, USA.
V PietroniLaboratory of Skin Biology, NIAMS, NIH, Bethesda, MD, USA.
N RadojaLaboratory of Skin Biology, NIAMS, NIH, Bethesda, MD, USA.
J HwangLaboratory of Skin Biology, NIAMS, NIH, Bethesda, MD, USA.
M BlumenbergDepartment of Dermatology, New York University, New York, NY, USA.ORCID 0000-0002-8672-7774
S H YuspaLaboratory of Cancer Biology and Genetics, NCI, NIH, Bethesda, MD, USA.
M I MorassoLaboratory of Skin Biology, NIAMS, NIH, Bethesda, MD, USA.
National Institute of Arthritis and Musculoskeletal and Skin Diseases · USCancer Genetics (United States) · USNew York University · US

Funding

Regulation Of Epidermal DifferentiationZIAAR041124 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI MORASSO, MARIA · 2009 to 2024
$21.1M
NIAMS Light Imaging FacilityZICAR041186 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI RANDAZZO, DAVIDE · 2010 to 2025
$18.2M
Interacting Signaling Pathways that Initiate Squamous Cell CarcinogenesisZIABC004504 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI YUSPA, STUART H. · 2009 to 2022
$15.7M
REGULATION OF EPIDERMAL DIFFERENTIATIONZ01AR041124 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI MORASSO, MARIA I · 2000 to 2008
$1.9M
Intramural NIH HHS Z01 AR041124Intramural NIH HHS ZIA AR041124
6 · The paper itself

Abstract

Epidermal homeostasis depends on the coordinated control of keratinocyte cell cycle. Differentiation and the alteration of this balance can result in neoplastic development. Here we report on a novel DLX3-dependent network that constrains epidermal hyperplasia and squamous tumorigenesis. By integrating genetic and transcriptomic approaches, we demonstrate that DLX3 operates through a p53-regulated network. DLX3 and p53 physically interact on the p21 promoter to enhance p21 expression. Elevating DLX3 in keratinocytes produces a G1-S blockade associated with p53 signature transcriptional profiles. In contrast, DLX3 loss promotes a mitogenic phenotype associated with constitutive activation of ERK. DLX3 expression is lost in human skin cancers and is extinguished during progression of experimentally induced mouse squamous cell carcinoma (SCC). Reinstatement of DLX3 function is sufficient to attenuate the migration of SCC cells, leading to decreased wound closure. Our data establish the DLX3-p53 interplay as a major regulatory axis in epidermal differentiation and suggest that DLX3 is a modulator of skin carcinogenesis.

Indexed as

AnimalsCarcinogenesisCarcinoma, Squamous CellCell Cycle CheckpointsCell DifferentiationCell ProliferationCyclin-Dependent Kinase Inhibitor p21Disease ProgressionFemaleHomeodomain ProteinsHumansMaleMiceSkin NeoplasmsTranscription FactorsTransfectionCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Distal-less homeobox proteinsHomeodomain ProteinsTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID26522723
PMCPMC4853298
OpenAlexW1897965600

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.